Augmented alpha‐adrenergic vasoconstriction during exercise in human metabolic syndrome

Abstract

The contribution of α‐adrenergic vasoconstriction during exercise in animal models of metabolic syndrome (MS) is controversial and the relevance to human MS is unclear. We hypothesized humans with MS (n=11) would exhibit greater α‐adrenergic vasoconstriction during exercise compared with healthy controls (n=16) and greater constriction would correlate with higher muscle sympathetic nerve activity (mSNA). We measured forearm blood flow (BF, Doppler ultrasound) and calculated changes in conductance (BF/blood pressure) with local intra‐arterial infusion of adrenergic agonists [phenylephrine (PE, α1), clonidine (CL, α2)] during dynamic forearm exercise (15% maximal effort). mSNA was measured in a subset of subjects (n=15, microneurography of the peroneal nerve). mSNA was higher in MS (66±9 vs 35±4 bursts/100 heart beats, p<0.01) and did not change with exercise. Infusion of PE decreased conductance similarly between groups. In contrast, MS subjects exhibited greater constriction to CL infusion compared with controls (p<0.01). Greater CL‐mediated constriction was associated with higher mSNA (r=0.51, p=0.05). These findings demonstrate greater α2‐adrenergic vasoconstriction during exercise in human MS which is related to higher mSNA. Such relationships may lead to impaired blood flow distribution and blood pressure regulation during exercise in MS. Support: AHA 10PRE3870000, NIH HL091397.